Chemotactic peptide stimulation of arachidonic acid release in HL60 cells, an interaction between G protein and phospholipase C mediated signal transduction.
Chemotactic peptide stimulation of arachidonic acid release in HL60 cells, an interaction between G protein and phospholipase C mediated signal transduction.
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趋化肽刺激 HL60 细胞中花生四烯酸的释放，这是 G 蛋白和磷脂酶 C 介导的信号转导之间的相互作用。
DOI：
10.1016/0167-4889(91)90048-3
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发表时间：
1991
期刊：
影响因子：
--
通讯作者：
Cockcroft,S
中科院分区：
文献类型：
--
作者：
Nielson,CP;Stutchfield,J;Cockcroft,S
为探讨趋化肽激活人早幼粒细胞磷脂酶A2的机制，用N-甲酰-甲硫基-亮氨酰-苯丙氨酸(FMetLeuPhe)和非水解型鸟苷类似物5‘-[γ-硫代]三磷酸(GTP[S])诱导渗透和代谢抑制的HL60细胞释放花生四烯酸，这是一种缓冲钙和抑制肌醇磷脂水解的制剂。肌醇磷酸生成和花生四烯酸在时间上是分离的。这些结果表明，fMetLeuPhe诱导花生四烯酸释放不需要依赖于受体的磷脂酶C活性。然而，fMetLeuPhe的作用是高度钙依赖的，即使在通透性的细胞制剂中，抑制磷脂酶C也会减少fMetLeuPhe对花生四烯酸释放的刺激。我们的结论是，虽然磷脂酶A2的激活与fMetLeuPhe受体有关，但磷脂酶C动员钙和释放二酰甘油的作用可能对完整细胞中的磷脂酶A2的激活很重要。
The mechanism of phospholipase A2activation by chemotactic peptide was investigated in human promyelocytic HL60 cells.N-Formyl-methionyl-leucyl-phenylalanine (fMetLeuPhe) and the non-Lydrolyzable GTP analogue guanosine 5′-[γ-thio]triphosphate (GTP[S]) induced arachidonic acid release in permeabilized and metabolically inhibited HL60 cells, a preparation in which calcium was buffered and inositol phospholipid hydrolysis was inhibited. Inositol phosphate generation and arachidonic acid were shown to be temporally dissociated. These results suggest that receptor-dependent phospholipase C activity is not required for fMetLeuPhe to induce arachidonic acid release. However, fMetLeuPhe effects were highly calcium-dependent and inhibition of phospholipase C reduced fMetLeuPhe stimulation of arachidonic acid release even in the permeabilized cell preparation. We conclude that although phospholipase A2activation is linked to the fMetLeuPhe receptor independent of phospholipase C, actions of phospholipase C to mobilize calcium and release diacylglycerol may be important to phospholipase A2activation in the intact cell.